Evidence map›Paper›PMID 27260854›Full record

ArticleCell cycle (Georgetown, Tex.)2016

FoxO1 antagonist suppresses autophagy and lipid droplet growth in adipocytes.

Longhua Liu, Louise D Zheng, Peng Zou, Joseph Brooke, Cayleen Smith, Yun Chau Long, Fabio A Almeida, Dongmin Liu, Zhiyong Cheng

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Review
  3. The link of FOXO1 and FOXO4 transcription factors to development of the lens.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Longhua Liua Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Louise D Zhenga Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Peng Zoua Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Joseph Brookea Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Cayleen Smitha Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Yun Chau Longb Department of Biochemistry , Yong Loo Lin School of Medicine, National University of Singapore , Singapore.
Fabio A Almeidaa Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Dongmin Liua Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Zhiyong Chenga Department of Human Nutrition, Foods, and Exercise , Fralin Life Science Institute, College of Agriculture and Life Science, Virginia Tech , Blacksburg , VA , USA.
Virginia Tech · USNational University of Singapore · SGUniversity of Nebraska Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and related metabolic disorders constitute one of the most pressing heath concerns worldwide. Increased adiposity is linked to autophagy upregulation in adipose tissues. However, it is unknown how autophagy is upregulated and contributes to aberrant adiposity. Here we show a FoxO1-autophagy-FSP27 axis that regulates adipogenesis and lipid droplet (LD) growth in adipocytes. Adipocyte differentiation was associated with upregulation of autophagy and fat specific protein 27 (FSP27), a key regulator of adipocyte maturation and expansion by promoting LD formation and growth. However, FoxO1 specific inhibitor AS1842856 potently suppressed autophagy, FSP27 expression, and adipocyte differentiation. In terminally differentiated adipocytes, AS1842856 significantly reduced FSP27 level and LD size, which was recapitulated by autophagy inhibitors (bafilomycin-A1 and leupeptin, BL). Similarly, AS1842856 and BL dampened autophagy activity and FSP27 expression in explant cultures of white adipose tissue. To our knowledge, this is the first study addressing FoxO1 in the regulation of adipose autophagy, shedding light on the mechanism of increased autophagy and adiposity in obese individuals. Given that adipogenesis and adipocyte expansion contribute to aberrant adiposity, targeting the FoxO1-autophagy-FSP27 axis may lead to new anti-obesity options.

Indexed as

3T3-L1 CellsAdipocytesAdipogenesisAdipose Tissue, WhiteAnimalsAutophagyCell DifferentiationCells, CulturedDown-RegulationForkhead Box Protein O1Lipid DropletsMacrolidesMaleMiceMice, Inbred C57BLProteins5-amino-7-(cyclohexylamino)-1-ethyl-6-fluoro-4-oxo-1,4-dihydroquinoline-3-carboxylic acidbafilomycin A1fat-specific protein 27, mouseForkhead Box Protein O1Foxo1 protein, mouseMacrolidesProteinsQuinolonesadipocyte expansionadipogenesisautophagy; FoxO1FSP27lipid droplet

Identifiers

PMID27260854
PMCPMC4968963
OpenAlexW2413000031

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.